The microRNA biogenesis machinery modulates lineage commitment during αβ T cell development.
Philadelphia, United States. In J Immunol, 15 Nov 2014
Dicer-deficient MHCI-restricted αβ T cells fail to normally silence Cd4 and display impaired induction of the CD8 lineage-specifying transcription factor Runx3, whereas Dicer-deficient MHCII-restricted αβ T cells show impaired Cd8 silencing and impaired induction of the CD4 lineage-specifying transcription factor Thpok.
CD4 CTL: living up to the challenge.
Los Angeles, United States. In Semin Immunol, Dec 2013
This lineage dichotomy is controlled by key transcription factors, including the T helper (Th) lineage master regulator, the Th-inducing BTB/POZ domain-containing Kruppel-like zinc-finger transcription factor, ThPOK, (formally cKrox or Zfp67; encoded by Zbtb7b), which suppresses the cytolytic program in major histocompatibility complex (MHC) class II-restricted CD4(+) thymocytes and the Runt related transcription factor 3 (Runx3), which counteracts ThPOK in MHC class I restricted precursor cells and promotes the lineage commitment of CD8αβ(+) cytolytic T lymphocytes (CTL).
The enigma of CD4-lineage specification.
Bethesda, United States. In Eur J Immunol, 2011
This review discusses recently identified nodes in the transcriptional circuits that are involved in controlling CD4(+) T-cell differentiation, notably the commitment factor Thpok and its interplay with Runx transcriptional regulators, and focuses on how transcription factors acting upstream of Thpok, including Gata3, Tox and E-box proteins, promote the emergence of CD4-lineage-specific gene expression patterns.
Identification of important regulatory region of Th-POK.
Tokushima, Japan. In J Med Invest, 2010
comparing the promoter regions of the Th-POK gene between human and mouse, the region 3600 base pairs upstream from the transcription initiation site of the Th-POK gene was highly conserved
Biology of the scleroderma fibroblast.
Boston, United States. In Curr Opin Rheumatol, 1998
In addition to these studies in scleroderma fibroblasts, work elucidating the role of transcription factors Sp1, Sp3, and cKrox in regulating collagen metabolism provided important data upon which future studies may build.